ArticleNucleic acids research2008
WRN Exonuclease activity is blocked by specific oxidatively induced base lesions positioned in either DNA strand.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Pigments from pathogenic bacteria: a comprehensive update on recent advances.World journal of microbiology & biotechnology · 2024Review
- Review
- Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.Ageing research reviews · 2017Review
- Induction of action-at-a-distance mutagenesis by 8-oxo-7,8-dihydroguanine in DNA pol λ-knockdown cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2015Article
- Human RecQ helicases in DNA repair, recombination, and replication.Annual review of biochemistry · 2014Review
- Cockayne Syndrome group B protein stimulates NEIL2 DNA glycosylase activity.Mechanisms of ageing and development · 2014Article
- The RECQL4 protein, deficient in Rothmund-Thomson syndrome is active on telomeric D-loops containing DNA metabolism blocking lesions.DNA repair · 2013Article
- Two novel PIWI families: roles in inter-genomic conflicts in bacteria and Mediator-dependent modulation of transcription in eukaryotes.Biology direct · 2013Article
- The Drosophila orthologue of progeroid human WRN exonuclease, DmWRNexo, cleaves replication substrates but is inhibited by uracil or abasic sites : analysis of DmWRNexo activity in vitro.Age (Dordrecht, Netherlands) · 2013Article
- Resolution of complex ends by Nonhomologous end joining - better to be lucky than good?Genome integrity · 2012Article
- Quantitative analysis of WRN exonuclease activity by isotope dilution mass spectrometry.Mechanisms of ageing and development · 2012Article
- Staphylococcus aureus DinG, a helicase that has evolved into a nuclease.The Biochemical journal · 2012Article
- DNA repair deficiency in neurodegeneration.Progress in neurobiology · 2011Review
- Non-B DNA-forming sequences and WRN deficiency independently increase the frequency of base substitution in human cells.The Journal of biological chemistry · 2011Article
- Roles of Werner syndrome protein in protection of genome integrity.DNA repair · 2010Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Werner syndrome (WS) is a premature aging disorder caused by mutations in the WS gene (WRN). Although WRN has been suggested to play an important role in DNA metabolic pathways, such as recombination, replication and repair, its precise role still remains to be determined. WRN possesses ATPase, helicase and exonuclease activities. Previous studies have shown that the WRN exonuclease is inhibited in vitro by certain lesions induced by oxidative stress and positioned in the digested strand of the substrate. The presence of the 70/86 Ku heterodimer (Ku), participating in the repair of double-strand breaks (DSBs), alleviates WRN exonuclease blockage imposed by the oxidatively induced DNA lesions. The current study demonstrates that WRN exonuclease is inhibited by several additional oxidized bases, and that Ku stimulates the WRN exonuclease to bypass these lesions. Specific lesions present in the non-digested strand were shown also to inhibit the progression of the WRN exonuclease; however, Ku was not able to stimulate WRN exonuclease to bypass these lesions. Thus, this study considerably broadens the spectrum of lesions which block WRN exonuclease progression, shows a blocking effect of lesions in the non-digested strand, and supports a function for WRN and Ku in a DNA damage processing pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.